Presentation description

Cardiovascular disease remains the leading cause of mortality in the elderly population, with limited treatment options beyond prevention. Aging is also associated with the substitution of beneficial gut microbes with opportunistic organisms that can promote the overproduction of harmful metabolites, such as trimethylamine-N-oxide (TMAO). TMAO is produced through microbial metabolism of dietary choline, phosphatidylcholine, and L-carnitine to trimethylamine (TMA), which is then oxidized in the liver by flavin monoxygenase 3 (FMO3). Elevated TMAO levels have been linked to metabolic disorders, including CVD, diabetes, and obesity. Studies from our lab indicate that dietary blueberries decrease TMAO accumulation in aged mice, although the exact mechanism is still unclear. In the current study, we investigated whether blueberries lower circulating TMAO by inhibiting FMO3 in aged mice. Adult mice (two months old) and old mice (17 months old) were fed a standard rodent diet. The subgroup of old mice was given a diet supplemented with 3.8% freeze-dried blueberries (~1.5 human servings) for 15 weeks. The liver samples were used to assess the expression of FMO3 by Western Blot. The preliminary findings suggest that blueberry supplementation reduces the expression of liver FMO3 in aged mice. Our ongoing studies are focused on confirming this result with more samples and assessing the microbial enzymes involved in the production of TMA. Our study will support the potential of blueberries as a dietary intervention to mitigate age-associated cardiometabolic risk.